Multiple Sclerosis (MS) is a presumed autoimmune disease of the central nervous system (CNS). Although etiology is unknown, it is thought to be incited by an environmental factor in a genetically susceptible host. Patients with MS tend to be immune hyper-responders, with enhanced T cell and /or B cell responses to a variety of antigens of host and infectious origin. This suggests an element of immune dysregulation in the pathogenesis of the disease. It has been demonstrated that specificity protein 3 (Sp3), a bifunctional transcription factor, is not expressed in the immune cells of patients with MS. Sp3 plays a role in the expression of various immune molecules such as anti-inflammatory cytokines and adhesion molecules. Hence, the lack of Sp3 expression could be a source of immune dysregulation in MS. Determining what surpresses the expression of Sp3 in MS immune cells will be accomplished by sequencing 5? flanking regions of the Sp3 gene, determining regulatory regions, and characterizing factors that bind to these regions in both MS and non-MS PBMCs. Ascertaining how Sp3 is surpressed in MS immune cells has potential etiological significance as well as therapeutic significance.